酸中毒和碱中毒课件.pptx

1、CaseCaseA 22-year-old woman who had been injured in an accident received 6 liters of isotonic saline, The plasma Na 135 mmol/l , K 3.8 mmol/l, Cl 115 mmol/l, and HCO3 18 mmol/l. The blood pH 7.28, and the PaCO2 39 mm Hg. The urinary sodium 65 mmol/l, potassium 15 mmol/l, and chloride 110 mmol/l. The

2、 patients serum albumin 2.7 g/dl after the infusion of saline. Her blood pressure was 98/52 mmHg, and her pulse rate was 102 beats/m.She had been healthy before the accident, was receiving no medications, and did not use any illicit drugs. The accident occurred when a speeding car ran through a red

3、light, hitting her car on the drivers side. The accident has caused multiple rib fractures, a compound left femoral fracture, a pelvic fracture, and numerous bruises. She is in the emergency department for stabilization of her condition before she can be sent to the operating room for stabilization

4、of her leg and pelvis.CaseA 22-year-old woman who had been injured in an accident received 6 liters of isotonic saline, The plasma Na 135 mmol/l , K 3.8 mmol/l, Cl 115 mmol/l, and HCO3 18 mmol/l. The blood pH 7.28, and the PaCO2 39 mm Hg. The urinary sodium 65 mmol/l, potassium 15 mmol/l, and chlori

5、de 110 mmol/l. The patients serum albumin 2.7 g/dl after the infusion of saline. Her blood pressure was 98/52 mmHg, and her pulse rate was 102 beats/m.She had been healthy before the accident, was receiving no medications, and did not use any illicit drugs. The accident occurred when a speeding car

6、ran through a red light, hitting her car on the drivers side. The accident has caused multiple rib fractures, a compound left femoral fracture, a pelvic fracture, and numerous bruises. She is in the emergency department for stabilization of her condition before she can be sent to the operating room

7、for stabilization of her leg and pelvis. 什么酸碱紊乱？什么酸碱紊乱？ 代谢、呼吸？代谢、呼吸？ AG酸中毒、高酸中毒、高氯氯性性 简单简单/复杂性？复杂性？Acid production in the bodyCarbonic acid:the metabolism of carbohydrates and fats (primarily derived from the diet) results in the production of approximately 15,000 mmol of CO2 per day. Non-carbonic a

8、cid:Organic: lactate, metabolized by the liver and kidneyInorganic:the metabolism of proteins and other substances results in the generation of noncarbonic acids (50 100 mEq, 1mEq/kg). Methionine glucose + urea + SO4(2-) + 2 H+ Arginine+ glucose (or CO2) + urea + H+ R-H2PO4 + H2O ROH + 0.8 HPO42- /

9、0.2 H2PO4- + 1.8 H+ The homeostatic response to acid load 1. Chemical buffering by the extracellular and intracellular buffers.2. Changes in alveolar ventilation to control the PCO2.3. Alterations in renal H+ excretion to regulate the plasma HCO3- concentration.Chemical buffering Extracellular buffe

10、rs Intracelluar: boneHenderson-Hasselbalch equation(Eq. 1) H+ + HCO3- H2CO3 H2O + CO2 PCO2(Eq. 2) H+ = 24 x HCO3-or by the Henderson-Hasselbalch equation HCO3-(Eq. 3) pH = 6.10 + log 0.03 PCO2 Henderson-Hasselbalch equation(Eq. 1) H+ + HCO3- H2CO3 H2O + CO2 PCO2(Eq. 2) H+ = 24 x HCO3-or by the Hende

11、rson-Hasselbalch equation HCO3-(Eq. 3) pH = 6.10 + log 0.03 PCO2Acidosis: PCO2=1.5 X HCO3 + 8 Chemical buffering Extracellular buffers Intracelluar buffer: bone, Ca+ release, osteoclast activationThe homeostatic response to acid load 1. Chemical buffering by the extracellular and intracellular buffe

12、rs.2. Changes in alveolar ventilation to control the PCO2.3. Alterations in renal H+ excretion to regulate the plasma HCO3- concentration.The homeostatic response to acid load 1. Chemical buffering by the extracellular and intracellular buffers.2. Changes in alveolar ventilation to control the PCO2.

13、3. Alterations in renal H+ excretion to regulate the plasma HCO3- concentration.RENAL HYDROGEN EXCRETION(1) reabsorption of the filtered HCO3-(2) excretion of the 50 to 100 meq of H+ produced per day1.Formation of titratable acid2.Excretion of NH4+ in the urineCollecting tubuleTubular LumenPeritubul

14、ar capillaryH+H2O2OH- + CO23HCO3-CAH+Cl-ATPaseATPaseH+K+Excretion of H+ in a intercalated cellsH+H+Collecting tubuleTubular LumenPeritubular capillaryH+H2O2OH- + CO23HCO3-CAH+HPO42-H2PO4Cl-ATPaseATPaseH+K+Excretion of H+ in a intercalated cellsCollecting tubuleTubular LumenPeritubular capillaryH+H2O

15、2OH- + CO23HCO3-CAH+NH3NH4+Cl-H+-ATPaseNH3Excretion of H+ in a intercalated cellsCan be stimulated by low KAcid-base balance The kidneys must excrete the 50 to 100 meq of noncarbonic acid generated each day. The daily acid load is excreted as NH4+ and H2(PO4). The daily acid load also cannot be excr

16、eted unless virtually all of the filtered HCO3- has been reabsorbed, because HCO3- loss in the urine is equivalent to adding H+ ions to the body. Regulation: The extracellular pH the effective circulating volume, aldosterone, and the plasma K+ concentrationCan be independent of serum pHSteps in acid

17、-base diagnosisObtain arterial blood gas (ABGs) and electrolytes simultaneouslyCompare HCO3-on ABGs and electrolytes to verify accuracyCalculate anion gap (AG)Know 4 causes of high AG acidosis Ketoacidsis Lactic acid acidosis Renal failure ToxinsKnow 2 causes of hyperchloremic or nongap acidosis Bic

18、arbonate loss from GI, RTAEstimate compensatory responseCompare AG and HCO3-Compare change in Cl with change in NaHenderson-Hasselbalch equation(Eq. 1) H+ + HCO3- H2CO3 H2O + CO2 PCO2(Eq. 2) H+ = 24 x HCO3-or by the Henderson-Hasselbalch equation HCO3-(Eq. 3) pH = 6.10 + log 0.03 PCO2Acidosis: PCO2=

19、1.5 X HCO3 + 8 Metabolic acidosis Influx of organic acid into plasma (high anion gap) Ketoacidosis Lactic acidosis Poisoning Accumulation of endogenous acids (high anion gap) Renal failure External losses of bicarbonate (normal anion gap; hyperchloremic). GI loss Renal lossAnion Gap AG=Na+-Cl-HCO3-

20、= 122 albumin: negative charged. Low serum albumin will reduce AG. Paraprotein (Ig or light chains, MM): positive charged. Presence of large amount of paraprotein reduces AG.Anion GapCauses of a High Anion Gap Metabolic AcidosisTypes and Causes of Lactic AcidosisTypes and Causes of Lactic AcidosisRe

21、nal failure With mild to moderate reductions in GFR, the acidosis reflects decreased ammoniagenesis and is therefore hyperchloremic. As kidney failure worsens, the kidney loses its ability to excrete various anions, and the accumulation of sulfate, phosphate, and other anions, produces an elevated A

22、G. Renal failure Despite a daily net positive acid balance, it is unusual for HCO3to fall lower than 15 mmol/L. The buffering of protons by bone results in loss of calcium and a negative calcium balance. Chronic acidosis causes protein breakdown, muscle wasting, and a negative nitrogen balance. Main

23、tenance of the acid-base balance close to normal can prevent these consequencesTreatment Alkali replacement NaHCO3 Sodium citrate Causes: Renal loss of alkali RTA GI loss of alkali Reciprocal changes in Cl and HCO3 result in normal AG In the absence of such a relationship suggests a mixed disturbanc

24、eDiarrhea Metabolic acidosis Metabolic acidosis and hypokalemia increase renal synthesis and excretion of NH4+, thus urinary pH is around 6 Urinary NH4 levels are high: urine anion gap is negativeProximal RTA (type 2) The threshold for HCO3- reabsorption in the proximal tubule is lower (normal: 26 -

25、28 mmol/l). The distal nephron has a low capacity for HCO3 reabsorption. Self-limited bicarbonaturia In the steady state, the serum HCO3 concentration usually is 16 18 mmol/l, when all the filtered HCO3 is reabsorbed. Despite systemic acidemia development, the urine pH is alkaline. However under ste

26、ady state, the urine can be acidified to a pH of less than 5.5.HCO3HCO3HCO3Proximal RTA: hypokalemia Increased distal Na+ delivery (NaHCO3) Increased aldosterone levels (dehydration because of loss of Na in the urine). Treatment of acidosis with HCO3 improves the acidosis but worsens the degree of h

27、ypokalemia.Causes of Proximal RTA Inherited pRTA: NBCe1/SLC4A4) mutation, accompanied by ocular abnormalities such as cataracts, glaucoma. Carbonic anhydrase inhibitor: acetazolamide Fanconi syndrome: inherited and acquired Adult with Fanconi: dysproteinemic condition such as multiple myelomadRTA (t

28、ype 1) Systemic acidosis in dRTA tends to be more severe than in patients with a proximal RTA (serum HCO3- can reach as low as 10 mmol/l vs 16 to 18 mmol/l) Hypokelemia can also be severe: musculoskeletal weakness Nephrolithiasis and nephrocalcinosisHCO3HCO3HCO3dRTA: kidney stone Urinary calcium exc

29、retion is high Acidosis induced bone mineral dissolution Low intraluminal concentration of HCO3- because of acidosis Urinary citrate levels are low citrate serve as the major Ca+ chelator in the urine High urine pH decrease the solubility of calcium phosphate complexes.dRTA Primary: idiopathic or in

30、herited (SLC4A1 mutation) Systemic disease: Sjogren syndromedRTA-diagnosis NH4Cl Furosemide + mineralocorticoid (fludrocortisone)dRTA Hyperchloremic acidosis Kidney stone Hypokalemia Sjogren syndromeType 4 RTA Renal function compromised Hyporeninemic hypoaldosteronism Hyperkalemia Urinary ammonium e

31、xcretion depressedMetabolic Alkalosis An elevated arterial pH An increase in the serum HCO3- and a increase in PCO2 Often accompanied by hypochloremia and hypokalemiaPathogenesis Generative stage: loss of acid Maintenance stage: volume contraction, a low GFR or depletion of Cl or KDifferential diagn

32、osis Mineralocorticoid excess Bartters or Gitelmans Diuretics Gastrointenstinal HCO3 retention + volume contraction Renal origin Diuretics Nonreaborbable anions and magnesium deficiency Potassium depletion After treatment of lactic acidosis or ketoacidosis posthypercapnia Mineralocorticoid administr

33、ation or excess production Symptoms: changes in central and peripheral nervous system function: confusion, obtundation, a predispositin to seizures Related electrolyte abnormalities: hypokalemia Treatment Correcting the underlying stimulus for HCO3 generation Removing the factors that sustain HCO re

34、absorption (ECFV contraction)Respiratory acidosis Severe pulmonary disease, respiratory muscle fatigue or abnormalities in ventilatory control Acute: immediate compensatory elevation in HCO3, which increases 1 mmol/L for every 10 mmHg increase in pCO2 Chronic (24h): renal adaptation increases the HC

35、O3 by 4 mmol/L Clinical features The clinical feature varies according to Severity and duration Underlying disease Whether there is hypoxemia A rapid increase in pCO2: anxiety, dyspnea, confusion coma Chronic hypercapnea: sleep disturbances, loss of memory, .Treatment Acute respiratory acidosis can

36、be life-threatening, measures to reverse the underlying cause should be undertaken simultaneously with restoration of adequate alveolar ventilation Chronic respiratory acidosis Improving lung functionRespiratory alkalosis Alveolar hyperventilation decreases PaCO2 and increases the HCO3/PCO2 When PaC

37、O2 is 40 15 mmHg, the relationship between arterial H+ and PaCO2 is about 0.7 mmol/L per mmHg, and that of plasma HCO3 is 0.2 mmol/ per mmHg Hypocapnia sustained longer than 2 to 6 h is further compensated by a decrease in renal ammonium and titratable acid excretion. Full renal adaptation may take

38、several days and require normal volume status and renal function The effect of respiratory alkalosis vary according to duration and severity but are primarily those of the underlying disease Hyperventilation syndrome Paresthesia, circumoral numbness, chest wall tightness, dizziness Salicylates are the most common cause of drug induced respiratory alkalosis Progesterone increases ventilation Respiratory alkalosis is often an early finding of G- septicemia